Current Pain and Headache Reports

, Volume 16, Issue 5, pp 433–438

Myofascial Pelvic Pain


    • Rhonda Kotarinos Physical Therapy, Ltd.
Myofascial Pain (RD Gerwin, Section editor)

DOI: 10.1007/s11916-012-0277-8

Cite this article as:
Kotarinos, R. Curr Pain Headache Rep (2012) 16: 433. doi:10.1007/s11916-012-0277-8


Myofascial pelvic pain is fraught with many unknowns. Is it the organs of the pelvis, is it the muscles of the pelvis, or is the origin of the pelvic pain from an extrapelvic muscle? Is there a single source or multiple? In this state of confusion what is the best way to manage the many symptoms that can be associated with myofascial pelvic pain. This article reviews current studies that attempt to answer some of these questions. More questions seem to develop as each study presents its findings.


Myofascial trigger pointMyofascial pain syndromeViscerosomatic convergenceSomatovisceral convergenceCentral sensitization


Chronic pelvic pain means many different things to different individuals. It is a general term encompassing an extremely diverse group of conditions: vulvodynia/vulvar vestibulitis, dyspareunia, interstitial cystitis/painful bladder syndrome, endometriosis, and chronic prostatitis/chronic pelvic pain syndrome to name a few. Hahn has described it as being associated with over 70 different diagnoses that often have overlapping physical, functional, and psychological components [1]. And that is just in women. It is estimated that chronic pelvic pain affects up to 15 % of women in the USA and the UK [2, 3]. Chronic prostatitis/chronic pelvic pain syndrome, as the condition is referred to in men, has a 2–10 % prevalence rate among adult men internationally [4].

There are many definitions for chronic pelvic pain and not one is generally considered acceptable. The American College of Obstetricians and Gynecologists defines chronic pelvic pain as pain of 6 or more month’s duration that is located in the abdomen, groin, or low back [5]. The International Continence Society’s definition is the occurrence of persistent or recurrent episodic pain associated with symptoms suggestive of lower urinary tract, sexual, bowel, or gynecologic dysfunction [6]. Chronic prostatitis/chronic pelvic pain syndrome as defined by a National Institute of Health Consensus is urologic pain or discomfort in the pelvic region that is associated with urinary symptoms and/or sexual dysfunction lasting for at least 3 of the previous 6 months [7]. Interesting how none of the definitions mention muscle as one of the body systems involved with chronic pelvic pain. Male or female, chronic pelvic pain is characterized by involving the pelvic cavity contents of the pelvic floor musculature [8]. It has only been in the recent past that muscles have been considered as a potential factor in the multifactorial etiology of chronic pelvic pain, in spite of the fact that Travell and Simons discussed the myofascial origins of chronic pelvic pain with and without viscerosomatic/somatovisceral reflex elements in their publications from 1983 and 1992 [9]. It was also in 1992 that Baskin and Tanagho ended a case series report with one extremely relevant suggestion, “However, it must be stressed that before extirpation of pelvic viscera organs is considered, pathological findings should be documented. The pelvic muscular element, which could well be the source of pain must be evaluated” [10]. Prior to this case series, Schmidt and Vapnek also implicated myofascial alterations and dysfunction as possible sources of chronic pelvic pain, specifically those associated with the lower urinary tract symptoms [11]. Slowly, ever so slowly the medical community is entertaining the concept of a myofascial component within the pelvis and/or lower quadrant as an etiologic source of chronic pelvic pain. The question then becomes what is the etiology of the myofascial dysfunction within myofascial pelvic pain.


The consensus is that myofascial trigger points are the most frequent cause of a regional myofascial pain syndrome [12, 13]. Active trigger points can develop as a result of mechanical, physical, organ system, and psychologial stressors [14]. Infertility treatments, rectal/vaginal ultrasound, colonoscopy, and childbirth are examples of events that can cause localized trauma resulting in a mechanical or physical stressor that can create myofascial trigger points. It is well established that myofascial trigger points can develop from more functional events through overuse, repetitive strains, motion injuries, or dysfunctional posturing as well as a result of a viscerosomatic reflex [9].

Herbert describes chronic pelvic pain as the “disease with 20 names” that may have interrelated physical, functional, and psychological etiologies [15]. This case series illustrates the challenges that many women have with obtaining a diagnosis and consequent management of chronic pelvic pain because of “the oft-overlooked role of nonphysiologic changes in body mechanics impacting somatic structures” [15]. With each case she describes how somatic imbalances can result in significant pain with the body’s compensatory changes developing into perpetuators of pain, thus demonstrating to the medical community the importance of somatic structures when organ centric sources of pain have been ruled out. Somatic structures directly related to the pelvis as well as those above and below that can refer to the pelvis and its contents must be considered when the clinician is examining a patient which they believe is experiencing myofascial pelvic pain. This was illustrated in Herbert’s case series with a patient that had a sudden onset of severe dysmenorrhea as a result of an ankle injury creating compensatory changes up the chain [15]. Correcting the compensatory changes and treating the ankle injury resolved the severe dysmenorrhea.

Diagnosing and managing chronic pelvic pain is difficult and confusing as a result of the many different and frequently divergent symptoms across several body systems. Hoffman expounds on an explanation for the multisymptom presentation of chronic pelvic pain [16]. This interpretation describes four possible explanations for the confusing presentation of chronic pelvic pain: viscerovisceral convergence, viscerosomatic convergence, hypertonicity of pelvic floor musculature, and central sensitization. Viscerovisceral convergence is the neural communication between viscera through the dorsal horn of the spinal cord; hence one pathological organ can create pathology in another organ via antidromic propagation of a neural impulse. Pezzone et al. referred to this as neural cross-talk, specifically, bidirectional cross-sensitization of the colon and lower urinary tract [17]. This concept provides an explanation of the overlap of symptoms between organ systems.

Viscerosomatic convergence is visceral pathology sending impulses to the dorsal horn of the spinal cord where they are conveyed to sympathetic and motor efferents resulting in changes in somatic tissues: skeletal muscle, skin, and blood vessels. Hoffman, citing Howard, explains that guarding reflexes are established as a result of pain felt from chronic inflammation or conditions such as endometriosis, ulcerative colitis, or chronic cystitis. The guarding reflex is an upregulation of sacral reflexes leading to muscle tightening and resultant pelvic floor dysfunction [18]. It definitely seems plausible that the constant holding of the muscles impacted by the guarding reflex is sufficient to create overload adequate to establish a myofascial trigger point. Think of the patient with a culture-proven cystitis who is experiencing that constant sense of urge, automatic inhibition has given way to active pelvic floor recruitment in an attempt to inhibit that urge. When they finally decide to void there is a distinct realization that there will be intense pain with voiding. Unable to fully relax the pelvic floor in anticipation of pain they void against a tightened pelvic floor setting up a trigger point that may persist long after the acute cystitis has resolved. From this point forward each time the pelvic floor is recruited to contract in a shortening or lengthening manner the active trigger point is irritated causing pain with urination without an infectious source. Hence, this could be a potential explanation for the symptoms of “chronic abacterial prostatitis” and interstitial cystitis.

Hypertonicity of the pelvic floor is also thought to be capable of creating visceral symptoms. Hoffman explains that direct mechanical compression of an organ and somatovisceral convergence can cause hypertonicity of the pelvic floor muscles. Even though she utilizes the generally accepted definition of a myofascial trigger point set forth by Travell and Simons [9], she goes on to state that they result in shortened muscles and produce hypertonicity. Motor dysfunction associated with a muscle with a trigger point is thought to be the result of inhibition [9]. Elevated EMG activity associated with a trigger point is only seen in the select muscle fibers associated with the trigger point and not the entire muscle. Should there be prolonged muscle recruitment as with a protective guarding reflex or chronic active recruitment for urge inhibition the pelvic floor can move into a state of contracture. With prolonged protective guarding the electrical generation eventually turns off and the muscle is left in a shortened state [19]. A physiologic contracture develops when the actin and myosin filaments cross-link remaining in a shortened state without motor unit action potentials [9]. A contracture of any skeletal muscle may establish conditions sufficient to create a myofascial trigger point.

If there is a physiologic contracture there is likely to be a clinical contracture. Clinical contractures develop when a muscle is maintained in a shortened state for a prolonged period of time resulting in remodeling of connective tissue creating fibrosis and sarcomeres are reduced [9]. In either case the contracture needs to be recognized and appropriately treated. The normal reflex response, as needed with urge inhibition or increased urethral closure pressure required with increased intra-abdominal pressure, may not be possible when a muscle is in the state of contracture. Symptoms that could be associated with a physiologic contracture of the pelvic floor musculature include the urologic symptoms associated with chronic pelvic pain syndromes such as frequency, urgency, and urge incontinence, not too mention the pain. Biofeedback is extremely effective in decreasing hypertonicity of muscle but cannot adequately address a contracture. Once the clinician determines they have an appropriate level of tone in the pelvic floor musculature, it may still be in a state of contracture and will require more advanced therapeutic techniques to address the pain and dysfunction.

Somatovisceral convergence, Hoffman’s third explanation of the multisymptom presentation of myofascial pelvic pain, is a result of noxious afferent impulses from muscle and other somatic tissues converging in the spinal cord causing antidromic impulses to the peripheral end organ [16]. Animal studies have demonstrated somatovisceral convergence. Clinically this can be seen when patients are overloading their abdominal wall with sit-ups for spring break creating myofascial trigger points that can refer to central pelvic organs. The saddle area of the lower trunk and the soft tissue of the suprapubic rim are areas known to be somatic referral zones to the bladder [20]. Trauma to this area such as with falls or cycling and seat belt trauma of a motor vehicle accident, respectively, could produce visceral symptoms.

Hoffman’s final explanation is the concept of central sensitization and the sensitized spinal segment. Musculoskeletal dysfunction that has pain sensitivity extending to deeper non-traumatized tissue with low-level peripheral impulses can establish central sensitization [21••]. Myofascial trigger points are the primary component of a regional myofascial pain syndrome. Many myofascial pain syndromes are known to be associated with central sensitization [22, 23]. Xu et al. recently demonstrated that persistent mechanical nociceptive stimulation of latent myofascial trigger points can initiate widespread central sensitization [24••]. Considering the previous patient scenario where a trigger point is established in the pelvic floor during acute cystitis, repeated voiding could be the persistent mechanical nociceptive stimulation establishing central sensitization and sensitized spinal segments.

In 2006, Langevin presented a question to the medical community regarding connective tissue functioning as a “whole body communication system” [25]. Langevin postulated that in order for connective tissue to act as a communication network there would have to be a signal generated by some part of connective tissue as a result of a precise stimulus with a signal being capable of transmission for some distance through the tissues. The potential signal sources that are mechanosensitive within connective tissue are cellular, electrical, and tissue remodeling [25]. Learning how connective tissue reacts to these three signals as well as the interaction between connective tissue and other tissues may provide an explanation as to how pathology in one area of the body “may cause a cascade of ‘remote’ effects in seemingly unrelated areas and organ systems” [25]. Stecco et al., while studying the histochemical distribution of hyaluronan, have found that the density of hyaluronan of loose connective tissue alters the behavior of the deep fascial layer [26•]. Therefore, the underlying muscles are unable to function optimally potentially being the source of myofascial pain. Is this the beginning of the evidence needed to answer the question regarding connective tissue as a comprehensive signaling network in the human body that may be the source of the many symptoms associated with myofascial pelvic pain? Even though the medical community is not certain of the etiology of myofascial pelvic pain, they need to at least consider a myofascial origin to the pelvic pain patient’s complaints and address it appropriately.


To diagnose a myofascial pelvic pain syndrome the clinician must be able to palpate a myofascial trigger point in extrapelvic as well as intrapelvic muscles. The muscle being examined is palpated perpendicular to its fiber orientation to locate a taut band. Palpation of the taut band continues parallel to the fiber orientation to locate the most painful spot. Regrettably, many researchers in myofascial pelvic pain describe pelvic floor muscle tenderness and do not provide the details of their evaluation technique [2730]. A literature review of pelvic pain in a urogynecology population was performed to describe definitions and the evaluation of pelvic pain [30]. Of 69 articles reviewed 20 % described a single-digit vaginal exam for myofascial trigger points, but the specifics of the technique were not elucidated. Another literature review of 60 articles regarding myofascial pelvic pain as a common urologic condition did not provide detailed specifics but did refer to myofascial trigger points being instrumental in the condition [31].

Bassaly et al. performed a retrospective chart review of patients diagnosed with interstitial cystitis to document whether or not myofascial trigger points were found and to correlate the myofascial exam results to validated questionnaires [32]. Of the 104 charts reviewed at least one myofascial trigger point was documented in 78.3 % and 67.9 % had six or more separate trigger points. Bassaly et al. did mention their evaluation technique, not in specific detail, acknowledging as a limitation of their study that a standardized palpation technique was difficult to achieve. This is in contrast to two randomized controlled clinical trials that did elucidate techniques, reporting excellence in standardization of the evaluation and treatment of urologic chronic pelvic pain patients [33••, 34••]. The myofascial trigger point as a significant factor in chronic pelvic pain will continue to be overlooked in the diagnostic workup until the evaluation process for trigger points is accepted and standardized across the medical disciplines.


Effective management of a condition that is clouded by confusion, unknown etiology, and the lack of standardization in its diagnostic process is difficult to say the least. Therapeutic options for myofascial pain according to Itza et al. is based upon myofascial release techniques combined with neuromuscular reeducation to inactivate trigger points [31]. Their review of articles summarized many multidisciplinary treatment options, but none of the studies were critically reviewed with regards to its level of evidence. Management options outlined by the review included prosto-centric treatment such as antibiotics, prostate massage, and intraprostatic injections. Specific medical management techniques for myofascial trigger points included local anesthetic, botulinum toxin, corticosteroid injections as well as dry needling. This was based upon six studies in spite of the fact that the results of the studies were contradictory: corticoids with local anesthetics do not improve clinical response, while another study stated corticosteroid injections should be a primary treatment. Physical therapy treatment for myofascial trigger points was described as passive stretching, manual release, and dry needling.

Lee and Lee did a systematic review of recent clinical studies to describe the utilization of acupuncture to treat chronic prostatitis/chronic pelvic pain syndrome [35]. Their belief is that acupuncture impacts the nervous system locally, segmentally, extrasegmentally, and centrally along with an impact on myofascial trigger points via a direct mechanical effect. After reviewing nine articles their conclusion was that acupuncture could be a safe and effective management option for the pain of chronic prostatitis/chronic pelvic pain but not for the urinary symptoms of quality of life. Even though trigger points were mentioned in the general discussion of acupuncture, they were not addressed in the review.

Botulinum toxins for the treatment of refractory chronic pain are a fairly new treatment option. Jabbari and Machado performed a systematic review on the utilization of botulinum toxins to treat chronic pain based upon prospective, randomized, double-blind placebo-controlled studies [36]. Their review analyzed only one double-blind controlled study on the use of onabotulinum toxin A for women with chronic pelvic pain. This study was labeled as Level C evidence as a result of the fact that primary and secondary outcomes were poorly defined. Eight randomized controlled trials of botulinum toxin for the treatment of myofascial pain syndrome were reviewed, none specific to the pelvis. These were labeled as Level U evidence indicating that there were insufficient findings to support or refute efficacy secondary to contradictory results.

The UPOINT system, reviewed by Doggweiler and Stewart, categorizes patients by symptoms that are then allocated to six different domains: urinary, psychosocial, organ specific, infection, neurologic/systemic, and skeletal muscle [37]. Myofascial trigger points and spasms are symptoms associated with the skeletal muscle domain. Organ specific, skeletal muscle, and urinary were the domains most frequently associated with the diagnosis of chronic pelvic pain syndrome. Treatment is then tailored to the individual to address their specific symptoms.

In a case series report, Anderson et al. present their results regarding the efficacy of a 6-day intensive treatment protocol that included internal/external manual myofascial trigger point release, instruction in self-management techniques (manual and instrumented), and paradoxical relaxation [38]. A total of 116 men were followed for 6 months. The ultimate goal of the study’s intervention was to adequately train the subjects to self-administer the treatment protocol, specifically trigger point manipulation and paradoxical relaxation. The global response assessment had an 82 % positive responder rate with 59 % marked or moderately improved and 23 % slightly improved. Focused myofascial trigger point therapy in conjunction with paradoxical relaxation within this case series was thought to be instrumental in addressing the refractory pain of chronic prostatitis/chronic pelvic pain syndrome. One positive aspect of this case series is that the myofascial release techniques were fully referenced allowing clinicians to incorporate them into their treatment armamentarium.

FitzGerald et al. published the results of a study that ascertained the feasibility of a randomized clinical trial of myofascial physical therapy for the treatment of urologic pelvic pain syndromes [33••]. Patients were randomized to two treatment arms: myofascial physical therapy which included evaluation and treatment of myofascial trigger points, connective tissue restrictions (subcutaneous panniculosis), neural mobilization/stretching and neuromuscular reeducation, and global therapeutic massage based upon the Swedish massage techniques of Frances Tappan. Determination of feasibility was based upon standardization of and adherence to the therapeutic protocol by the physical therapists as determined by treatment records, adverse events, and the global response assessment. A larger scale randomized trial was determined to be feasible based upon the patients being willing to be randomized, and standardization and adherence to both treatment protocols were achieved. Adverse events were as expected that was evidenced by a low dropout rate. Clinically the most significant outcome was the positive responder rate as determined by the global response assessment, which was 57 % for the myofascial physical therapy arm as compared to 21 % for the massage arm. This was the first and only positive treatment trial in 10 years of National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) funded research for urologic chronic pelvic pain.

Encouraged by the strong positive outcome of the feasibility study a full-scale clinical trial of myofascial physical therapy was initiated. The aim of this study was to determine the efficacy and safety of myofascial physical therapy as compared to global therapeutic massage in women with recent-onset symptomatic interstitial cystitis/painful bladder syndrome [34••]. As with the feasibility one of the strongest positive outcomes of this study was the ability to standardize and adhere to an evaluation and treatment protocol of myofascial trigger points and other soft tissue dysfunction. The positive responder rate on the global response assessment of this trial was 59 % for the physical therapy arm and 26 % for the massage arm. Unfortunately, the secondary endpoints of symptom questionnaires and Likert scales for pain and urge did not confirm the primary endpoints. In spite of this result, this was the second positive randomized controlled trial for a disorder that is in desperate need of effective and safe treatment options. The ultimate culmination of these two randomized clinical trials was the American Urological Association Guideline: Diagnosis and Treatment of Interstitial Cystitis/Bladder Pain Syndrome listing myofascial physical therapy as the first choice of second-line treatment [39••].


It is well established that there are a lot of unknowns in the etiology, pathophysiology, assessment, and management of myofascial trigger points and their related myofascial pain syndromes. This is ever so true for the presentation of myofascial pelvic pain. Fragmentation of health care has limited advances in this area of study but does seem to be changing as there are more studies encompassing multidisciplinary teams. Research continues to stress that all chronic pelvic pain patients should be subjected to a full evaluation of the urologic, gastroenterologic, neurologic, and finally being considered more consistently, the musculoskeletal organ system.


No potential conflicts of interest relevant to this article were reported.

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© Springer Science+Business Media, LLC 2012